The role of the hypermetabolic response, observed in patients and experimental animals with extensive thermal injury, will be investigated with special emphasis on its relationship to cellular metabolism. The experiments are designed to establish mechanisms responsible for inhibition of active transport of sodium following burn injury and prolonged negative energy balance. The pathophysiology resulting from inhibition of neutrophil function and abnormal coagulation dynamics will also be evaluated in burned patients. Finally, the role of plasma amino acid alterations in initiating the hypermetabolic response will be assayed. Experimental methods employed include in vitro measurement of cellular membrane transport of glucose and sodium, in vitro assessment of aerobic and anaerobic organ metabolism, fractionation of fibrin split products isolated from burned animals and patients, and amino acid analysis. Amino acid radioactive tracer studies will be utilized to evaluate specific utilization of the branch chain amino acids and small animal direct calorimetry will be developed to assess energy requirements in the animal burn model.